Chapter 13. Memory, Learning, and Development

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 61 - 80 of 6083

By NICHOLAS BAKALAR Chronic inflammation in middle age may be associated with an increased risk for brain shrinkage and Alzheimer’s disease later in life. A new study, published in Neurology, looked at 1,633 people whose average age was 53 in 1987-89, measuring white blood cell count and various blood proteins that indicate inflammation. They followed the participants for 24 years. In 2011-13, when the subjects’ average age was 77, the scientists measured their brain volume using M.R.I. and tested their mental agility with a word-memorization task. They found that the greater the number of elevated inflammatory markers earlier in life, the smaller the volume of several parts of the brain, including those associated with Alzheimer’s disease. Higher levels of inflammation were also associated with poorer performance on the memory test. The authors acknowledge that they had blood tests for only one point in time, and that they are assuming that brain loss occurred in the years after the inflammatory markers were assessed. “It’s important early in life that we prevent diseases like diabetes, heart disease or hypertension that cause systemic inflammation,” said the lead author, Keenan A. Walker, a postdoctoral fellow at Johns Hopkins. “This study shows a temporal relationship between early inflammation and later brain volume loss.” © 2017 The New York Times Company

Keyword: Alzheimers; Neuroimmunology
Link ID: 24277 - Posted: 11.02.2017

Using an innovative “NeuroGrid” technology, scientists showed that sleep boosts communication between two brain regions whose connection is critical for the formation of memories. The work, published in Science, was partially funded by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a project of the National Institutes of Health devoted to accelerating the development of new approaches to probing the workings of the brain. “Using new technologies advanced by the BRAIN Initiative, these researchers made a fundamental discovery about how the brain creates and stores new memories,” said Nick Langhals, Ph.D., program director at NIH’s National Institute of Neurological Disorders and Stroke. A brain structure called the hippocampus is widely thought to turn new information into permanent memories while we sleep. Previous work by the new study’s senior author, New York University School of Medicine professor György Buzsáki, M.D., Ph.D., revealed high-frequency bursts of neural firing called ripples in the hippocampus during sleep and suggested they play a role in memory storage. The current study confirmed the presence of ripples in the hippocampus during sleep and found them in certain parts of association neocortex, an area on the brain’s surface involved in processing complex sensory information. “When we first observed this, we thought it was incorrect because it had never been observed before,” said Dion Khodagholy, Ph.D., the study’s co-first author and assistant professor at Columbia University in New York.

Keyword: Learning & Memory
Link ID: 24274 - Posted: 11.01.2017

Teens are getting less sleep than they did before smartphones became commonplace, prompting concerns about potentially serious health consequences, researchers say. A study published in the current issue of the journal Sleep Medicine examined data from two surveys of U.S. adolescents conducted over many years and including questions about how many hours of sleep they got. Almost 370,000 adolescents participated. The researchers focused on how much sleep teens reported getting in the years from 2009 to 2015, "when the mobile technology really saturated the market among adolescents," said Zlatan Krizan, a psychologist specializing in sleep and social behaviour at Iowa State University and co-author of the study. Zlatan Krizan, a psychology researcher specializing in sleep, personality and social behaviour at Iowa State University, was one of the authors of a recent study that showed a trend of teens getting less sleep over the years they started using smartphones. (Iowa State University) Krizan and his colleagues found that teens were 16 to 17 per cent more likely to report getting less than seven hours of sleep a night in 2015 than they were in 2009. The recommended amount of sleep for 13 to 18-year-olds is eight to 10 hours per night, according to the U.S. Centers for Disease Control and Prevention. ©2017 CBC/Radio-Canada.

Keyword: Sleep; Development of the Brain
Link ID: 24273 - Posted: 11.01.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Keyword: Schizophrenia; Depression
Link ID: 24270 - Posted: 10.31.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Keyword: Alzheimers; Prions
Link ID: 24266 - Posted: 10.31.2017

There is no good evidence that a nutrient drink being sold online in the UK to "help" people with early Alzheimer's actually slows the disease, say experts. Latest trial results in patients who took Souvenaid did not find it preserves memory and thinking. The authors say in Lancet Neurology that bigger studies are needed to show if the product can work as hoped. And consumers should be aware that the £3.49 per bottle drink "is not a cure". Manufacturer Nutricia says its drink should only be taken under the direction of a doctor, specialist nurse or pharmacist. Souvenaid comes in strawberry or vanilla flavour and contains a combination of fatty acids, vitamins and other nutrients. Taken once daily, the idea is that the boost of nutrients it provides will help keep Alzheimer's at bay in people with the earliest signs of this type of dementia. But the latest phase two clinical trial results do not prove this. What the trial found The study involved 311 patients with very early Alzheimer's or mild cognitive impairment. All of them were asked to take a daily drink, but only half were given Souvenaid - the other half received one with no added nutrients. After two years of participating, the patients were reassessed to see if there was any difference between the two groups in terms of dementia progression, measured by various memory and cognitive tests. The treatment did not appear to offer an advantage, although patients in the Souvenaid group did have slightly less brain shrinkage on scans, which the researchers say is promising because shrinkage in brain regions controlling memory is seen with worsening dementia. But experts remain cautious. Prof Tara Spires-Jones, a dementia expert at the University of Edinburgh, said: "Some of the other tests of brain structure and function were promising, but overall this study indicates that a specific change in nutrition is unlikely to make a large difference to people with Alzheimer's, even in the early stages. © 2017 BBC.

Keyword: Alzheimers
Link ID: 24265 - Posted: 10.31.2017

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 24264 - Posted: 10.30.2017

By Michael Ellenbogen Twenty years ago, at age 39, I began having memory and cognitive problems. My primary-care doctor and my neurologists said I was stressed and depressed. I also was diagnosed with mild cognitive impairment, or MCI. Ten years later, I received another diagnosis. Well, really two. One doctor said I had Alzheimer’s disease, and another thought it was semantic dementia. Alzheimer’s is a devastating chronic neurodegenerative disease. It is a progressive mental deterioration that advances to affect bodily functions such as walking and swallowing, and always leads to death. Semantic dementia leads to losses of vocabulary, fluency of speech and meanings of familiar words. It also is progressive. After another year of testing, physicians decided that I had Alzheimer’s. While it was a relief to finally get a diagnosis, I realized that I had been given a death sentence. There is no prevention or cure for Alzheimer’s, and no survivors. Overwhelmed, I decided to help the search for a cure by advocating for Alzheimer’s and dementia. I got involved with clinical trials and advocacy. My huge network on LinkedIn allowed me to connect with advocates and information. It gave me access to many tests, including gene tests, free. Two contacts — health-care professionals — even read my medical records and scans and gave me their opinions. Alzheimer’s is a complex disease to diagnose. The science is just not there yet. Sixty to 80 percent of dementia cases are said to be due to Alzheimer’s. But postmortem tests of elderly patients have found that dementia has several causes. s. © 1996-2017 The Washington Post

Keyword: Alzheimers
Link ID: 24260 - Posted: 10.30.2017

By Corinna Hartmann, Andreas Jahn Medical historians have recently published accounts that show neurologists were indeed complicit with the Nazis—and became victims if they were classified as “non-Aryan. Heiner Fangerau, who teaches the history and ethics of medicine at University Hospital Düsseldorf—along with colleagues Michael Martin at the Heinrich Heine University of Düsseldorf and Axel Karenberg from the University of Cologne—undertook extensive research on neurologists during the Third Reich for the German Society of Neurology. Fangerau discussed new findings with Corinna Hartmann and Andreas Jahn of Gehirn&Geist, the psychology and neuroscience specialty publication of Spektrum der Wissenschaft, and the German sister publication of Scientific American. An edited transcript of the interview follows. Professor Fangerau, your research project examines the role played by neurologists during the Nazi period. Why is this only happening 70 years after the fact? Advertisement There were several different phases in which people dealt with National Socialism after World War II. Immediately after 1945 the Allies pursued a policy of denazification. After that German society as a whole attempted to suppress its dark past. Many members of the next generation, however, found it impossible to close their eyes: Students in the 1968 movement were angry that their parents were unwilling to deal openly with the “Third Reich.” The medical specialties took even longer to begin working through the past. As a result, their reappraisal of the crimes committed began only in the 1980s. Part of the reason why historical research into neurology has only been conducted systematically over the past several years is that neurology and psychiatry were forced into the same disciplinary framework in 1935. Before then neurology had begun to separate from psychiatry. The basic idea was to leave psychological phenomena that are difficult to understand to the psychiatrists and to concentrate on disorders that are anatomically demonstrable. The National Socialists nullified this effort. They believed that they could control these medical specialties more effectively if they brought them together in the Society of German Neurologists and Psychiatrists, which was dominated by psychiatrists committed to the ideology of racial hygiene. The chairman of the society was Ernst Rüdin, a psychiatrist. As a result, neurology has come to be viewed as less implicated. Historical research conducted since the late 1980s, however, paints a very different picture. © 2017 Scientific American

Keyword: Genes & Behavior
Link ID: 24238 - Posted: 10.25.2017

By Renee Joy Dufault, Steven G. Gilbert According to the CDC, autism prevalence continues to climb with 8 year old boys afflicted 4.5 times more often than girls. What makes matters worse is the fact that many boys with autism are also diagnosed with ADHD. These disorders severely impact the learning process in the classroom environment and lead to a lifelong economic burden both for the afflicted individual and society. Researchers estimated the annual economic burden in the U.S. for autism alone in 2015 was $162-$367 billion. If the autism prevalence continues to rise, researchers predict the costs will likely exceed those of ADHD and diabetes by 2025. It is imperative that families receive the support they need to prevent and manage these disorders which often occur in tandem. Proper management requires an understanding of the causes or “risk factors.” One cause associated with both disorders is exposure to heavy metals found in a poor diet. Heavy metal exposures may occur from the consumption of highly processed foods that contain ingredients with allowable concentrations of lead and inorganic mercury. Furthermore, these heavy metals may accumulate in blood especially when diet does not include adequate minerals to support the gene activity needed to metabolize and excrete them. Researchers led by Alabdali recently found higher blood lead and mercury levels are correlated with the severity of social and cognitive impairment in children with autism. What this means is parents will have more difficulty managing their child with autism and ADHD as the mercury and/or lead concentration levels rise in his blood. © 2017 Scientific American

Keyword: Autism; Sexual Behavior
Link ID: 24234 - Posted: 10.24.2017

Jon Hamilton When it comes to brain training, some workouts seem to work better than others. A comparison of the two most common training methods scientists use to improve memory and attention found that one was twice as effective as the other. The more effective method also changed brain activity in a part of the brain involved in high-level thinking. But neither method made anyone smarter, says Kara Blacker, the study's lead author and a researcher at The Henry M. Jackson Foundation for the Advancement of Military Medicine in Bethesda, Md. "Our hypothesis was that training might improve fluid intelligence or IQ," Blacker says. "But that's not what we found." Blacker did the memory research when she was part of a team at Johns Hopkins University and the Kennedy Krieger Institute in Baltimore. The results were reported in the Journal of Cognitive Enhancement. The team compared two approaches to improving working memory, which acts as a kind of mental workspace where we store information temporarily. "If somebody gives you directions, you have to keep that information in mind long enough to actually execute going to that location," Blacker says. "If someone tells you a phone number, you have to be able to remember it." To test different methods for improving working memory, the team had 136 young adults spend a month training their brains for 30 minutes a day, five days a week. Johns Hopkins University YouTube One group did something called a "complex span" test, which involves remembering the location of an item despite distractions. A second group trained with something called the dual n-back test. Each day they would sit at a computer watching flashing squares appear on a grid and listening to a voice reading letters from the alphabet. © 2017 npr

Keyword: Learning & Memory; Attention
Link ID: 24231 - Posted: 10.23.2017

By Alice Klein Four genes have been identified that are linked to obsessive compulsive disorder (OCD). The genes all play a role in the same brain circuit, and may help explain why people are more likely to have OCD if they have a relative with the condition. People with OCD have intrusive thoughts and feel driven to repeat rituals, such as handwashing, to relieve their anxiety. To investigate if OCD has a genetic basis, Hyun Ji Noh at the Broad Institute of MIT and Harvard and her colleagues compared more than 600 genes across 592 people with OCD, and 560 people who don’t have it. They chose these candidate genes from several lines of evidence. Of these genes, 222 had been linked to compulsive grooming in mice, and 196 had been linked to autism in people – a condition that can involve repetitive behaviours. The team also looked at 56 genes that they had identified in a study of dogs with canine compulsive disorder, a condition in which dogs repeatedly chase their tails, pace back and forth, groom themselves or sucks things, sometimes for hours at a time. Brain safety circuit The analysis identified four genes that are different in people who have OCD. All four of these are active in a brain circuit that links the striatum, thalamus and cortex regions. © Copyright New Scientist Ltd.

Keyword: OCD - Obsessive Compulsive Disorder; Genes & Behavior
Link ID: 24210 - Posted: 10.18.2017

Jon Hamilton Brain imaging studies have a diversity problem. That's what researchers concluded after they re-analyzed data from a large study that used MRI to measure brain development in children from 3 to 18. Like most brain imaging studies of children, this one included a disproportionate number of kids who have highly educated parents with relatively high household incomes, the team reported Thursday in the journal Nature Communications. For example, parents of study participants were three times more likely than typical U.S. parents to hold an advanced degree. And participants' family incomes were much more likely to exceed $100,000 a year. So the researchers decided to see whether the results would be different if the sample represented the U.S. population, says Kaja LeWinn, an assistant professor at the University of California, San Francisco School of Medicine. "We were able to weight that data so it looked more like the U.S." in terms of race, income, education and other variables, she says. And when the researchers did that, the picture of "normal" brain development changed dramatically. For instance, when the sample reflected the U.S. population, children's brains reached several development milestones much earlier. © 2017 npr

Keyword: Brain imaging; Development of the Brain
Link ID: 24204 - Posted: 10.17.2017

By Rhianna Schmunk, CBC News Researchers from the University of British Columbia are retracting their scientific paper linking aluminum in vaccines to autism in mice, because one of the co-authors claims figures published in the study were deliberately altered before publication — an issue he says he realized after allegations of data manipulation surfaced online. The professor also told CBC News there's no way to know "why" or "how" the figures were allegedly contorted, as he claims original data cited in the study is inaccessible, which would be a contravention of the university's policy around scientific research. The paper looked at the effects of aluminum components in vaccines on immune response in a mouse's brain. It was published in the Journal of Inorganic Biochemistry on Sept. 5. Co-authored by Dr. Chris Shaw and Lucija Tomljenovic, it reported aluminum-triggered responses "consistent with those in autism." Shaw said he and Tomljenovic drew their conclusions from data that was "compiled" and "analyzed" for the paper, rather than raw data. However, subsequent scrutiny has raised questions about the validity of the data, with one doctor calling the paper "anti-vaccine pseudoscience." By the middle of September, commenters on PubPeer — a database where users can examine and comment on published scientific papers — pointed out that figures in the study appeared to have been altered, and in one case lifted directly from a 2014 study also authored by Shaw and Tomljenovic. ©2017 CBC/Radio-Canada.

Keyword: Autism
Link ID: 24199 - Posted: 10.16.2017

by Sari Harrar, AARP Bulletin, At 99 years old Brenda Milner continues to explore the mind and its relationship to people’'s behavior. You'’re a preeminent neuroscientist, and a professor at Canada's prestigious McGill University. At age 99, what motivates you to keep up your research at the Montreal Neurological Institute and Hospital? I am very curious. Human quirks attract my interest. If you’'re a theoretical person, you can sit and dream up beautiful theories, but my approach is, “What would happen if …”or, “Why is this person doing [that] …”and then, “How can I measure it?” I wouldn't still be working if I didn't find it exciting. AARP Membership: Join or Renew for Just $16 a Year Are you curious in real life, too? Yes. I'm a good "noticer—" of behavior as much as the kind of furniture people have! In the 1950s, you made a revolutionary discovery— that memories are formed in a brain area called the hippocampus, which is now getting lots of attention for its role in memory loss and dementia. Has brain research gotten easier? Nowadays, everyone has functional magnetic resonance imaging. Anybody with access to a medical school can get a good look at the patients' brain while they're alive and young, but it wasn't like that [then]. Psychologists were studying patients who were much older and beginning to show memory impairment. Then they had to wait for their patients to die.

Keyword: Learning & Memory
Link ID: 24196 - Posted: 10.16.2017

By Virginia Morell Dog owners often wonder what—if anything—is going on when their pooches are sleeping. It turns out they may be learning, according to a new study. Researchers in Hungary trained 15 pet dogs to sit and lie down using English phrases instead of the Hungarian they already knew. Afterward, the scientists attached small electrodes to the dogs’ heads to record their brain activity while they slept. Electroencephalograms (EEGs) showed that during 3-hour naps, the dogs’ brains experienced brief, repeated moments of “slow-wave” brain activity, lasting 0.5 to 5 seconds. These bursts—called sleep spindles because they look like a train of fast, rhythmic waves on EEG recordings—occur during non-REM sleep and are known to support memory, learning, general intelligence, and healthy aging in humans and rats. But this is the first time they’ve been studied in detail in dogs. Like those of humans and rats, the dogs’ sleep spindles occur in short cycles in the 9-hertz to 16-hertz range; in humans and rats, these cycles are associated with memory consolidation. The scientists also discovered that the number of spindle sessions per minute correlated with how well the dogs learned their new, foreign vocabulary, the researchers report this week in Scientific Reports. And—just like in humans—females had more spindle sessions per minute than males and performed better during testing. About 30% of the females learned the new words, compared to about 10% of the males. That suggests, the researchers say, that dogs can serve as models to better understand the function of our own sleep spindles. © 2017 American Association for the Advancement of Science

Keyword: Sleep; Learning & Memory
Link ID: 24191 - Posted: 10.14.2017

Laura Sanders The brain’s mapmakers don’t get a break, even for sleep. Grid cells, specialized nerve cells that help keep people and other animals oriented, stay on the clock 24/7, two preliminary studies on rats suggest. Results from the studies, both posted October 5 at bioRxiv.org, highlight the stability of the brain’s ‘inner GPS’ system. Nestled in a part of the brain called the medial entorhinal cortex, grid cells fire off regularly spaced signals as a rat moves through the world, marking a rat’s various locations. Individual grid cells work together to create a mental map of the environment. But scientists didn’t know what happens to this map when an animal no longer needs it, such as during sleep. Grid cells, it turns out, maintain their mapmaking relationships even in sleeping rats, report two teams of researchers, one from the University of Texas at Austin and one from the Norwegian University of Science and Technology in Trondheim. (The Norway group includes the researchers who won a Nobel Prize in 2014 for discovering grid cells (SN Online: 10/6/14).) By eavesdropping on pairs of grid cells, researchers found that the cells maintain similar relationships to each other during sleep as they do during active exploration. For instance, two grid cells that fired off signals nearly in tandem while the rat was awake kept that same pattern during sleep, a sign that the map is intact. The results provide insights into how grid cells work together to create durable mental maps. © Society for Science & the Public 2000 - 2017.

Keyword: Learning & Memory
Link ID: 24186 - Posted: 10.13.2017

By Emily Underwood If you’ve ever found yourself in an MRI machine, you know keeping still isn’t easy. For newborns, it’s nearly impossible. Now, a portable, ultrasonic brain probe about the size of a domino could do similar work, detecting seizures and other abnormal brain activity in real time, according to a new study. It could also monitor growing babies for brain damage that can lead to diseases like cerebral palsy. “This is a window of time we haven’t had access to, and techniques like this are really going to open that up,” says Moriah Thomason, a neuroscientist at Wayne State University in Detroit, Michigan, who wasn’t involved in the new study. Researchers have long been able to take still pictures of the newborn brain and study brain tissue after death. But brain function during the first few weeks of life, which is “utterly essential to future human health,” has always been something of a black box, Thomason says. Two techniques used in adults—functional magnetic resonance imaging (fMRI), which can measure blood flow; and electroencephalography (EEG), which measures electrical activity in the outer layers of the brain—have their drawbacks. FMRI doesn’t work well with squirmy tots, is expensive, and is too big to haul to a delicate baby’s bedside. EEG—which only requires attaching a few wires to someone’s head—can’t penetrate deeper brain structures or show where a seizure begins, critical information for doctors weighing treatment options, says Olivier Baud, a developmental neuroscientist at the Robert Debré University Hospital in Paris. © 2017 American Association for the Advancement of Science.

Keyword: Brain imaging; Development of the Brain
Link ID: 24183 - Posted: 10.12.2017

By Esther Landhuis Among hundreds of genes that might nudge your risk of Alzheimer's up or down, Apolipoprotein E (APOE) has the strongest effect. Scientists discovered a quarter century ago that people with the APOE ε4 version of this gene are four to 15 times more likely to develop Alzheimer’s, a deadly brain disorder that afflicts more than five million Americans. Yet how APOE actually sets off dementia has been somewhat of a mystery—and efforts to use it as a drug target have floundered. The field’s attention has focused on another “A” word—amyloid beta (Aβ). This protein can unwittingly accrue in the brain for years, disrupting nerve connections essential for thinking and memory. APOE has been thought of as a co-conspirator in this process, but finding ways to undermine its collusion have proved challenging. Anti-amyloid drugs have consumed the labors of pharmaceutical companies. If a drug could break those insidious clumps of protein or keep them from forming, drug developers reasoned, it could in theory halt the progression of the disease. But billions of dollars have poured into large-scale clinical trials of amyloid-lowering therapies that so far have failed. Advertisement APOE has hovered on the periphery as far as drug development, but this could soon change. Connections have emerged between the functioning of APOE and Aβ. In 2012 Boston scientists studying autopsy tissue from Alzheimer’s patients found APOE ε4 individuals had unusually high levels of brain Aβ. And they noticed Aβ clumped more readily in test tubes if mixed with ApoE proteins, especially ApoE4. Mouse data from teams at Washington University in Saint Louis and the University of California, San Francisco—suggested a similar relationship. Each lab worked with existing Alzheimer’s mouse models and further modified their genomes to make different types and amounts of ApoE proteins. In both studies animals with less ApoE had fewer Aβ plaques in their brains. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 24176 - Posted: 10.12.2017

By NICHOLAS BAKALAR Women with high blood pressure in their 40s are at increased risk for dementia in later years, researchers report. But the finding does not hold for men. Beginning in 1964, investigators collected health and lifestyle information on 5,646 men and women when they were 30 to 35 years old, and again when they were in their 40s. From 1996 to 2015, 532 of them were found to have Alzheimer’s or other forms of dementia. The study is in Neurology. Hypertension in women in their 30s was not associated with dementia. But women who were hypertensive at an average age of 44 had a 68 percent higher risk for dementia than those who had normal blood pressure at that age, even after adjusting for B.M.I., smoking and other risk factors. High blood pressure in men in their 30s or 40s was not associated with later dementia, but the study’s senior author, Rachel A. Whitmer, said that studies have tied hypertension in men in their 50s to later dementia. Dr. Whitmer, a senior research scientist at Kaiser Permanente in Oakland, Calif., added that hypertension is more common in men, and the hypertensive men in the study tended to die at a younger age than the women. “The big picture here is that brain health is a lifelong issue,” she said. “What you do in young adulthood matters for your brain in old age.” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 24175 - Posted: 10.12.2017